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H Tsukagoshi

Publications and source records attributed to H Tsukagoshi.

At least 37 records · Page 2Linked to original sources
PubMed1999

Cecal ligation and puncture peritonitis model shows decreased nicotinic acetylcholine receptor numbers in rat muscle: immunopathologic mechanisms?

BACKGROUND: Although systemic inflammation is believed to cause upregulation of nicotinic acetylcholine receptors (nAchRs) in muscle, chronic infections such as Chagas' disease occasionally are complicated by myasthenia gravis. The authors investigated how a nonlethal cecal ligation and puncture (CLP) peritonitis model in rats could affect muscle nAchR. METHODS: On day 1, 4, 7, 14, or 21 after CLP or sham operation, nAchR binding was assayed in the anterior tibial muscle and diaphragm using [125I]alpha-bungarotoxin. The presence or absence of weakness, in vivo dose-response relationships for d-tubocurarine, and serum anti-nAchR antibody titers were assayed in separate experiments. RESULTS: Systemic inflammation was most severe during the first 4 to 5 days. Numbers of nAchRs were decreased in anterior tibial muscle on days 7, 14, and 21 after CLP, and in the diaphragm on days 7 and 14 (P < 0.01). Both 50% and 90% blocking doses of d-tubocurarine) were lower in CLP rats than in sham-operated rats on days 7, 14, and 21 (P < .05). Weakness was overt in approximately half of CLP rats at these times. Serum anti-nAchR antibody (0.7-1.4 nM) was detectable beginning on day 4 and continuing throughout the 21-day observation period in 58-67% of CLP rats. CONCLUSIONS: During the recovery phase of injury, nonlethal CLP peritonitis resulted in downregulation of nAchR. However, further study is needed to determine the role of anti-nAchR antibodies in the development of decreased receptor numbers and impaired neuromuscular function.

Animals↗
PubMed1999

Comparison of the hemodynamic effects of amrinone in patients who required low-to-moderate-dose and high-dose catecholamines after cardiac valve replacement.

OBJECTIVES: To determine hemodynamic response to amrinone in patients after cardiac surgery, in relation to the postoperative cardiac function, which was indicated by the required doses of catecholamines. DESIGN: Prospective clinical study. SETTING: Surgical intensive care unit in a university hospital. PATIENTS: Fourteen patients who required a low-to-moderate dose of dopamine and dobutamine (group L) and 14 patients who required a high dose of dopamine and dobutamine (group H) after cardiac valve replacement. INTERVENTIONS: A loading dose of amrinone (0.75 mg/kg) was administered during a 15-min period and the continuous infusion was followed incrementally by doses of 5, 10, and 20 microg/kg/min every 60 mins on the first postoperative day. MEASUREMENTS AND MAIN RESULTS: Hemodynamic variables were determined by the radial and pulmonary artery catheters at a dose of 0, 5, 10, and 20 microg/kg/min. Two-way repeated-measures analysis of variance showed significant interaction in the two groups in cardiac index and mean systemic arterial pressure. Cardiac index increased in a dose-dependent manner in group L but was unchanged in group H. Systemic vascular resistance index decreased in a dose-dependent manner in both groups. The mean systemic arterial pressure decreased in group L at a dose of 5 microg/kg/min and returned to the baseline level at doses of 10 and 20 microg/kg/min. On the other hand, the mean systemic arterial pressure significantly decreased in group H at a dose of 20 microg/kg/min. CONCLUSIONS: The inotropic effects of amrinone after cardiac valve replacement may be associated with the postoperative myocardial reserve, which was indicated by the required doses of catecholamines, although a similar vasodilative effect was observed in both groups.

Adult↗
PubMed1998

A possible involvement of oxidative lung injury in endotoxin-induced bronchial hyperresponsiveness to substance P in guinea pigs.

Reactive oxygen-derived free radical species have been implicated in the pathogenesis and pathophysiology of inflammatory lung diseases. In a guinea pig model of aerosolized endotoxin-induced bronchial hyperresponsiveness to substance P, a possible involvement of oxidative lung injury was assessed by measuring the changes in membrane-bound neutral endopeptidase activity in the airway tissues and the level of lipid peroxides in the plasma. Vehicle-treated animals developed a neutrophilic airway inflammation, bronchial hyperresponsiveness to substance P associated with neutral endopeptidase hypoactivity, and elevation of lipid peroxides at 18 to 24 h after an exposure to endotoxin (75 microgram/ml, 40 min). A nonselective phosphodiesterase inhibitor, aminophylline, and selective phosphodiesterase isoenzyme inhibitors, SDZ-ISQ-844 (type III/IV) and SDZ-MKS-492 (type III), attenuated the neutrophilic airway inflammation induced by endotoxin. Aminophylline, SDZ-MKS-492, and a superoxide anion-generating NADPH-oxidase inhibitor apocynin inhibited bronchial hyperresponsiveness to substance P with attenuation of neutral endopeptidase inactivation induced by endotoxin. SDZ-ISQ-844, SDZ-MKS-492, and apocynin attenuated the elevation of lipid peroxides. The generation of hypochlorite (OCl-) from whole blood leukocytes was attenuated by aminophylline, SDZ-ISQ-844, SDZ-MKS-492, and apocynin at 1 to 2 h after exposure. These results suggest that reactive oxygen-derived free radical species-mediated oxidative lung injury may play an important role in endotoxin-induced bronchial hyperresponsiveness to substance P, and that phosphodiesterase isoenzyme inhibitors may be potentially useful as anti-inflammatory drugs.

Acetophenones↗
PubMed1998

Kimura's disease associated with bronchial asthma presenting eosinophilia and hyperimmunoglobulinemia E which were attenuated by suplatast tosilate (IPD-1151T).

A 29-year-old man developed atopic bronchial asthma in association with eosinophilia and hyperimmunoglobulinemia E (hyper-IgE). A biopsy specimen from an inguinal lymph node showed changes consistent with Kimura's disease. IPD-1151T (suplatast tosilate), an anti-allergy drug, attenuated eosinophilia and hyper-IgE as well as the serum level of eosinophil cationic protein (ECP). The drug, however, did not affect the positivity for specific IgE antibodies against common allergens or the bronchial hyperresponsiveness to acetylcholine. Interleukin (IL)-2, IL-4, IL-5, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha were measured to be undetectable in serum before or during therapy. However, the expressions of mRNAs for IL-2, IL-4, IL-5, IFN-gamma, and TNF-alpha in peripheral blood T-lymphocytes and the expression of IL-5 mRNA in peripheral blood eosinophils were detected before and during therapy, which were unchanged by therapy with IPD-1151T. The present results suggest that different mechanisms other than the predominance of type 2 helper (T(H2))-like T-lymphocytes may underlie Kimura's disease and atopic bronchial asthma regarding the findings of eosinophilia and hyper-IgE, which could be modulated by IPD-1151T.

Adult↗
PubMed1998

An autopsy case of systemic hemangiomatosis with honeycomb-like liver and focal splenic sarcomatoid changes.

An unusual autopsy case of systemic hemangiomatosis associated with honeycomb-like liver and splenic sarcomatoid changes is presented. The patient suffered from high-output ventricular heart failure secondary to hepatic arteriovenous shunting with hepatic failure, ending fatally due to disseminated intravascular coagulation and pulmonary bleeding. Postmortem examination revealed the characteristic distribution of vasoformative tumors presenting in the hematopoietic system including the liver, bone marrow, and spleen, with the liver appearing characteristically honeycomb-like. While these vasoformative tumors were mostly benign-appearing, partial shifts toward sarcomatoid change were observed in the splenic lesions.

Angiomatosis↗
PubMed1997

Spinocerebellar ataxia type 6: CAG repeat expansion in alpha1A voltage-dependent calcium channel gene and clinical variations in Japanese population.

Autosomal dominant spinocerebellar ataxias (SCAs) are clinically and genetically a heterogeneous group of neurodegenerative disorders. Recently, mild CAG repeat expansion in the alpha1A voltage-dependent calcium channel gene has been found to be associated with a type of autosomal dominant SCA (SCA6). We analyzed 98 Japanese families with autosomal dominant SCAs, for whom CAG repeat expansions of the SCA1, SCA2, Machado-Joseph disease/SCA3, and dentatorubral-pallidoluysian atrophy genes were excluded, and 5 apparently sporadic cases of cortical cerebellar atrophy. The diagnosis of SCA6 was confirmed in 30 families (31%) comprising 47 affected individuals and 1 sporadic case. The size of expanded CAG repeats ranged from 21 to 26 repeat units and was found to be correlated inversely with age at onset. We identified 2 SCA6 patients homozygous for expanded CAG repeats, whose ages at onset were earlier than the 95% lower confidence level, suggesting the presence of a gene dosage effect of expanded CAG repeat. Ataxia is the most common initial symptom found in 45 of the 48 patients. Patients with a prolonged disease course showed other accompanying clinical features including dystonic postures, involuntary movements, and abnormalities in tendon reflexes.

Adult↗
PubMed1997

Effects of the calcium ionophore A23187 on airway responsiveness to histamine and substance P in guinea pigs.

OBJECTIVE: We evaluated the mechanism of the airway hyperresponsiveness (AHR) induced by a calcium ionophore in guinea pigs. MATERIALS AND METHODS: Airway responsiveness to intravenous histamine (HS) and substance P (SP) was measured 24 h after a 1-h exposure to aerosolized A23187 (0.03 or 0.1 mg/ml) or its vehicle (10% DMSO). Changes were assessed by calculating -logPC350HS and logPC350SP. Neutral endopeptidase (NEP) activity in the airway tissues, as well as the nitrite (NO2) levels and the cell population in bronchoalveolar lavage fluid (BALF) was determined after measurement of pulmonary function. Changes in SP-induced vascular permeability 24 h after exposure to A23187 were measured by the Evans Blue dye extravasation technique. RESULTS: Exposure to A23187 caused a significant AHR to SP, along with a significant increase in the number of neutrophils and epithelial cells in the BALF. While there was no significant change in NEP activity in the airway tissues, the levels of nitrite in the BALF were significantly decreased in A23187-exposed animals. Significant correlations were found between the number of epithelial cells in the BALF and logPC350SP (r = 0.477, p < 0.05) and between nitrite levels in the BALF and -logPC350SP (r = 0.491, p < 0.05) A23187 exposure did not significantly change the SP-induced airway microvascular leakage. CONCLUSIONS: These data suggest that A23187 exposure induced AHR to SP possibly by reducing NO levels in the airway tissues. This may be due to damaged airway epithelium and/or NO breakdown by activated inflammatory cells in the airways of these guinea pigs.

Animals↗
PubMed1997

Adoptive transfer of allergen-specific CD4+ T cells induces airway inflammation and hyperresponsiveness in brown-Norway rats.

Following allergen exposure, sensitized Brown-Norway rats develop airway hyperresponsiveness (AHR) and eosinophilic inflammation together with an increase in activated T cells (CD25+) in the airways. We tested the hypothesis that CD4+ T cells are involved directly in the acquisition of AHR. Spleen T cells from animals that were injected intraperitoneally on three consecutive days with ovalbumin/Al(OH)3, showed a dose-dependent proliferative response in vitro to ovalbumin, but not to bovine serum albumin, as measured by [3H]thymidine uptake. For total T-cell transfer, spleen cells obtained from donor rats 4 days after sensitization were depleted of adherent cells by a nylon wool column separation. CD4+ and CD8+ T cells were purified by immunomagnetic beads cell separation. Recipient naive rats were injected intravenously with 50 x 10(6) total T cells, 20 x 10(6) and 5 x 10(6) CD4+ cells, and 5 x 10(6) CD8+ cells, and were exposed to ovalbumin aerosol 24 hr afterwards. After a further 24 hr, airway responsiveness to acetylcholine (ACh) was measured and provocative concentration (PC) values PC100, PC200 and PC300) (the ACh concentration needed to achieve 100, 200 and 300% increase in lung resistance above baseline) were calculated. Airway responsiveness was significantly increased in recipients of sensitized total T cells compared with recipients of cells from saline-injected donor rats (P < 0.05). There were significantly increased eosinophil major basic protein (MBP)+ cell counts/mm2 in airway submucosal tissue in the hyperreactive rats and a significant correlation was found between the number of MBP+ cells and PC100 (r = 0.75; P < 0.03) in recipients of sensitized total T cells. Purified CD4+ T cells from sensitized donors induced AHR in naive recipients (P < 0.05), while sensitized CD8+ and naive CD4+ cells failed to do so. Our data indicate that T cells may induce AHR through an eosinophilic airway inflammation and that CD4+ T cells may have a direct effect in this process in Brown-Norway rats.

Adoptive Transfer↗
PubMed1997

Factors affecting neostigmine reversal of vecuronium block during sevoflurane anaesthesia.

We examined the influence of the concentration of sevoflurane and the degree of muscle block at the time of reversal on the activity of neostigmine. Ninety ASA 1-2 patients were anaesthetised with 0.2, 0.7 or 1.2 MAC of sevoflurane (30 patients each) in 66% nitrous oxide in oxygen. The electromyographic (EMG) response of the adductor digiti minimi was monitored at 20-s intervals after train-of-four stimulation of the ulnar nerve. The initial neuromuscular block was produced by vecuronium 100 micrograms.kg-1. When the amplitude of the first response (T1) values had recovered to 10%, 25% or 40% of the control, neostigmine 40 micrograms.kg-1 was administered. The train-of-four ratio values were recorded at 1-min intervals during the subsequent 15-min period. Higher endtidal concentrations (p < 0.0001) and more pronounced block at the time of reversal (p < 0.0001) were associated with a delayed recovery in the train-of-four ratio. In addition, the train-of-four ratio 15 min after neostigmine administration was more dependent on the sevoflurane concentration than on the degree of block present (p < 0.0001). These results confirm that neostigmine (40 micrograms.kg-1) can reverse vecuronium-induced but not sevoflurane-induced neuromuscular block.

Adult↗
PubMed1996

Sevoflurane and isoflurane impair edrophonium reversal of vecuronium-induced neuromuscular block.

PURPOSE: A dose-response relationship study for edrophonium to examine the modification of volatile anaesthetics on reversal of vecuronium block. METHODS: One hundred and twenty ASA (I-II) patients were anaesthetized with sevoflurane, isoflurane (1 minimum alveolar anaesthetic concentration [MAC] end-tidal concentration), or fentanyl-diazepam anaesthesia, in combination with 66% nitrous oxide (n = 40 for each group). The evoked electromyogram (EMG) response of the abductor digiti minimi was monitored at 20 sec intervals following train-of-four (TOF) stimulation of the ulnar nerve. The initial neuromuscular block was produced by vecuronium 100 micrograms.kg-1. When the amplitude of the first response (T1) had spontaneously recovered to 10% of the control, edrophonium (0, 125, 400, 700 or 1000 micrograms.kg-1; eight patients each) was randomly administered, and the ratio of the fourth TOF to the first response (TOFR) was monitored at one minute intervals for 10 min. RESULTS: Sevoflurane and isoflurane impaired the edrophonium-assisted TOFR recovery in an edrophonium dose and time dependent manner. The dose-response curves at 10 min exhibited a greater shift to the right in the sevoflurane and isoflurane groups than in the fentanyl-diazepam-nitrous oxide group (P < 0.05). Higher ED50 values (the edrophonium dose required to obtain TOFR value of 50%) in the sevoflurane (> 1000 micrograms.kg-1) and isoflurane groups (851 micrograms.kg-1) were observed than in the fentanyl-diazepam-nitrous oxide group (339 micrograms.kg-1) (P < 0.05). CONCLUSION: One MAC sevoflurane and isoflurane anaesthesia impair edrophonium reversal of vecuronium block to a similar degree.

Adult↗
PubMed1996

Changes of unmyelinated nerve fibers in sural nerve in amyotrophic lateral sclerosis, Parkinson's disease and multiple system atrophy.

Quantitative changes in unmyelinated nerve fibers (UMNFs) of sural nerves in patients of amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD) and multiple system atrophy (MSA) were evaluated using autopsy materials whose pathological diagnosis had been confirmed by careful postmortem examinations. Ordinary ALS cases demonstrated no involvement in cutaneous UMNFs; however, the patients with long survival due to the application of ventilatory support showed bimodality in UMNF diameter histograms, and a patient with involvement of systems other than motor pathways showed an abnormal value in two indices: a low percentage of subunits containing axon(s) and a high mean number of Schwann cell profiles per axon. A significant reduction of the mean value of UMNF density (21%) was found in PD patients. Because the density of myelinated nerve fibers did not show any significant decrease as compared with age-matched controls, the change of nerve fibers in peripheral nervous system was considered to be confined to UMNFs in PD. Elderly PD cases showed enhanced changes in the ageing process, as expressed by the two indices described above. In MSA, the mean value of UMNF density was significantly decreased (23%), and this decrease almost paralleled that of myelinated nerve fiber density. Abnormal values for the two indices described above were found and two out of four cases demonstrated bimodality in the diameter histogram of UMNFs. Unlike MSA, ALS and PD have not been included in the disorders with cutaneous UMNF involvement. Our results supply the first evidence of morphological changes in cutaneous UMNFs in PD cases. In ordinary ALS cases, the emergence of such morphological changes is suggested in cases with long survival.

Age Distribution↗
PubMed1996

CV6209 inhibits airway wall thickening and airway hyperresponsiveness to histamine induced by intravenous administration of platelet-activating factor in guinea pigs.

We studied the effect of intravenous administration of platelet-activating factor (PAF) on airway responsiveness to histamine and airway wall thickening in guinea pigs. Guinea pigs were killed and the lungs were fixed in formalin. Slides from paraffin-embedded sections of the lungs were stained and the airways that were cut in transverse section were measured by tracing enlarged images using a digitizer. Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyzer and we calculated two indices, an index of airway wall thickening and one of airway hyperresponsiveness to histamine, from changes of baseline-Raw and peak-Raw following intravenous administration of histamine before and after PAF administration. The infusion of 600 ng/kg PAF for 1 h induced an increase in the thickness of the airway wall in main bronchi demonstrable by histological examination. In analysis of airway function, the infusion of 600 ng/kg PAF for 1 h induced airway hyperresponsiveness to histamine with airway wall thickening. The PAF antagonist CV6209, which was given intravenously 30 min prior to PAF administration, inhibited these effects of PAF in a dose-dependent manner, suggesting PAF may induce airway wall thickening and airway hyperresponsiveness through PAF receptors in the airways.

Airway Resistance↗
PubMed1995

Inadequate antagonism of vecuronium-induced neuromuscular block by neostigmine during sevoflurane or isoflurane anesthesia.

To examine the effects of discontinuing sevoflurane or isoflurane anesthesia (1 minimum alveolar anesthetic concentration [MAC] of end-tidal concentrations, together with 66% N2O/O2) on the reversal of vecuronium-induced neuromuscular blockade (an initial dose = 100 micrograms/kg), the electromyographic response of the abductor digiti minimi was monitored at 20-s intervals after train-of-four (TOF) stimulation of the ulnar nerve in 192 ASA grades I and II patients. When the amplitudes of the first response (T1) had recovered to 10% of the control, neostigmine (0;spontaneous recovery, 10, 20, 30, 40, or 55 micrograms/kg, eight patients each) was given and the ratio of the fourth TOF to the first response (TOFR) was monitored at 1-min intervals for 15 min in the presence of the volatile anesthetics, or after discontinuation of anesthetic administration. Spontaneous TOFR recovery was also assessed in another eight patients who were anesthetized with 66% N2O/O2-fentanyl-diazepam. Adequate antagonisms (TOFR > 75%) were achieved after discontinuation of both administrations, but not during anesthetic administration at the neostigmine doses tested. The dose-response curves for neostigmine (10, 20, 30, and 40 micrograms/kg) were constructed using the TOFR values at 5-11 min, from which the ED50 values (a neostigmine dose required for a TOFR value of 50%) were derived. Sevoflurane impaired neostigmine antagonism more than isoflurane, as demonstrated by the significantly higher ED50 values at 7-11 min (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Induction of macrophage inflammatory protein 2 gene expression by interleukin 1 beta in rat lung.

BACKGROUND: Recruitment of inflammatory cells in the lungs may contribute to tissue injury as a result of mediators released from these cells. Interleukin 1 beta (IL-1 beta) is a potent inducer of neutrophil accumulation, a process that may require local protein biosynthesis. Macrophage inflammatory protein 2 (MIP-2) is a approximately 6 kD heparin binding protein and is a member of the C-X-C superfamily that causes significant neutrophil chemotaxis and activation in vitro. A study was performed to determine whether IL-1 beta could induce the expression of MIP-2 in the lungs of Brown-Norway rats. METHODS: rhIL-1 beta (500 U) or 0.9% NaCl was injected intratracheally and bronchoalveolar lavage (BAL) cells and lung tissues were evaluated for MIP-2 mRNA expression after RNA extraction by Northern blot analysis. MIP-2 probe was prepared from cDNA obtained by reverse transcriptase-polymerase chain reaction (RT-PCR) of BAL cells obtained from a rat treated with lipopolysaccharide. RESULTS: There was no detectable MIP-2 mRNA in the lungs of control rats but a marked enhancement of the expression at four hours with no expression at 12 hours and a slight expression at 24 hours. IL-1 beta induced a significant influx of neutrophils into BAL fluid with a transient increase in macrophages. In situ hybridisation of lungs using MIP-2 cDNA probe labelled with digoxigenin showed expression of MIP-2 mRNA in airway mononuclear cells and airway epithelium at four hours after IL-1 beta; at 24 hours the signal had nearly gone. CONCLUSION: IL-1 beta induces the expression of MIP-2 mRNA in rat lung. MIP-2 may be one chemokine that could contribute to IL-1 beta induced neutrophil influx.

Animals↗
PubMed1995

Ozone-induced airway hyperresponsiveness: role of superoxide anions, NEP, and BK receptors.

We investigated the role of reactive oxygen species in ozone-induced airway hyperresponsiveness (AHR) in Brown Norway rats. Airway responsiveness to inhaled acetylcholine (ACh) and bradykinin (BK) and inflammatory cell recruitment in bronchoalveolar lavage fluid (BALF) were measured in vivo. Neutral endopeptidase (NEP) activity assay and measurement of BK-receptor binding sites in Brown Norway rat lungs were carried out in vitro. Apocynin (5 mg/kg), an inhibitor of superoxide anion-generating NADPH oxidase, was administered perorally 30 min before a 3- or 6-h exposure to 3 ppm of ozone, and the animals were studied 18-24 h postexposure. Ozone induced increases in airway responsiveness to ACh and BK and in neutrophil counts in BALF. Apocynin inhibited the increase in airway responsiveness to BK but not to ACh without affecting the neutrophil counts in BALF. The antioxidants allopurinol and deferoxamine prevented ozone-induced AHR to both ACh and BK but did not reduce neutrophil counts. To further examine the mechanisms of ozone-induced AHR to BK, we measured NEP activity and the density of BK receptors in vitro after ozone exposure. Ozone exposure had no significant effect either on NEP activity or on the affinity and the number of BK receptors in lungs from rats treated with or without apocynin. We conclude that superoxide anions released from inflammatory cells in the airway may be involved in ozone-induced AHR. Inactivation of NEP or upregulation of BK receptors do not appear to be involved, but the possibility of localized changes cannot be excluded.

Acetylcholine↗
PubMed1995

Role of neutral endopeptidase in bronchial hyperresponsiveness to bradykinin induced by IL-1 beta.

Interleukin-1 beta (IL-1 beta) induces bronchial hyperresponsiveness (BHR) to bradykinin but not to acetylcholine. We examined whether this was mediated through the inhibition of neutral endopeptidase (NEP) activity and/or through the enhancement of airway microvascular leakage (AML) by IL-1 beta. We administered human recombinant IL-1 beta (500 U) or saline intratracheally and 24 h later measured the airway responses to bradykinin (1 mM; 45 breaths). IL-1 beta-treated rats showed a decrease of 18.5 and 21.1% of NEP activity in the lungs and tracheobronchial tree, respectively (P < 0.05), associated with an augmented response in total lung resistance to bradykinin but with no increase in Evans blue dye extravasation used as a marker of AML. Phosphoramidon (0.1 and 1 mM; 90 breaths), an NEP inhibitor, induced a dose-dependent increase in lung resistance to bradykinin without further enhancing BHR induced by IL-1 beta. Bradykinin-induced AML was not enhanced by phosphoramidon in either saline- or IL-1 beta-treated rats. Similarly, after captopril (1 mM; 90 breaths), an inhibitor of angiotensin-converting enzyme, there was no further enhancement of BHR to bradykinin induced by IL-1 beta. BHR to bradykinin induced by IL-1 beta may result from an inhibition of peptidase activity, such as NEP and angiotensin-converting enzyme, and is not associated with an enhancement of AML.

Administration, Inhalation↗
PubMed1995

Evaluation of influential factors of cognitive impairments in idiopathic Parkinson's disease.

Using multivariate analysis, we investigated the influence on cognitive functions of aging, brain atrophy, incidental cerebral hyperintensities (CHs), medication, and severity, duration and the initial symptoms of the disease in 53 patients with idiopathic Parkinson's disease (PD). We semiquantitatively assessed the degree of brain atrophy and CHs based on previously established methods. Cognitive functions were significantly and diffusely impaired in PD when compared with controls who were matched for age as well as for the degree and location of CHs. Patients with PD, however, had larger ventricles. Prefrontal dysfunctions were associated with a variety of predictors such as CHs, brain atrophy, severity of PD and medication whereas dorsolateral frontal functions were related simply to age and CHs in the periventricular region. Posterior brain functions had association with severity of illness, ventricular dilatation and total CH score. Clinically observed cognitive impairments in PD may consist of cognitive defects intrinsic to the disease which are variously modified by these factors. It is essential to consider all these predictors simultaneously in any discussion of cognitive functions in PD.

Aged↗